Morroniside plays a therapeutic role in knee osteoarthritis (OA) by protecting chondrocytes. PI3K/AKT signaling is involved in the regulation of chondrocytes by Morroniside. PI3K/AKT suppresses autophagy through downstream signaling. However, the regulation of chondrocyte autophagy by Morroniside and the significance of the above effect on protecting chondrocytes aren't clear. The results showed that Morroniside inhibited the autophagiy of human OA chondrocytes. Besides, both PI3K inhibitors and mTOR inhibitors significantly reversed the autophagy reduced by Morroniside, but had no effect on the protective effect of Morroniside on chondrocytes. However, the enhanced autophagy caused by overexpression of autophagic genes enhanced the protective effect of Morroniside on chondrocytes. In conclusion, Morroniside represses the autophagy of human OA chondrocyte, which is related to PI3K/mTOR pathway. Moreover, the upregulation of autophagy further promoted the role of Morroniside in treating chondrocytes. Our data present a potential clue for the therapeutic strategies of Morroniside in treating OA.

中文翻译：

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促进自噬增强莫诺苷对人 OA 软骨细胞的保护作用。


莫诺苷通过保护软骨细胞在膝骨关节炎 (OA) 中发挥治疗作用。 PI3K/AKT 信号传导参与莫诺苷对软骨细胞的调节。 PI3K/AKT 通过下游信号传导抑制自噬。然而，莫诺苷对软骨细胞自噬的调节作用以及上述作用对保护软骨细胞的意义尚不清楚。结果表明，莫诺苷抑制人OA软骨细胞的自噬。此外，PI3K抑制剂和mTOR抑制剂均显着逆转莫诺苷减少的自噬，但对莫诺苷对软骨细胞的保护作用没有影响。然而，自噬基因过度表达引起的自噬增强增强了莫诺苷对软骨细胞的保护作用。总之，莫诺苷抑制人OA软骨细胞的自噬，其与PI3K/mTOR通路有关。此外，自噬的上调进一步促进了莫诺苷治疗软骨细胞的作用。我们的数据为莫诺苷治疗 OA 的治疗策略提供了潜在的线索。